Strategic Grassland Bird Conservation throughout the Annual Cycle: Linking Policy Alternatives, Landowner Decisions, and Biological Population Outcomes

<div><p>Grassland bird habitat has declined substantially in the United States. Remaining grasslands are increasingly fragmented, mostly privately owned, and vary greatly in terms of habitat quality and protection status. A coordinated strategic response for grassland bird conservation is difficult, largely due to the scope and complexity of the problem, further compounded by biological, sociological, and economic uncertainties. We describe the results from a collaborative Structured Decision Making (SDM) workshop focused on linking social and economic drivers of landscape change to grassland bird population outcomes. We identified and evaluated alternative strategies for grassland bird conservation using a series of rapid prototype models. We modeled change in grassland and agriculture cover in hypothetical landscapes resulting from different landowner decisions in response to alternative socio-economic conservation policy decisions. Resulting changes in land cover at all three stages of the annual cycle (breeding, wintering, and migration) were used to estimate changes in grassland bird populations. Our results suggest that successful grassland bird conservation may depend upon linkages with ecosystem services on working agricultural lands and grassland-based marketing campaigns to engage the public. With further development, spatial models that link landowner decisions with biological outcomes can be essential tools for making conservation policy decisions. A coordinated non-traditional partnership will likely be necessary to clearly understand and systematically respond to the many conservation challenges facing grassland birds.</p></div

Resulting hypothetical grassland bird population growth rates over a 30-year time period, in response to various policy alternatives.

<p>Results indicate different potential impacts of policies, varying by landowner types, in relation to the percentage of grassland cover in the landscape.</p

Preference weights for each landowner type, for each objective and policy.

<p>Weights were used to evaluate land cover choices for each landowner and were based on the opinions of workshop participants. Future applications of this approach could incorporate empirical social science data to inform the value weightings of an agent-based model.</p

The effect of each policy and landowner on the expected growth of grassland bird populations where alternatives and values were determined by workshop participant expert opinion.

<p>Values indicate average population growth rates, per year, after a 30-year simulation period, in response to the respective policy alternatives, for each landowner type.</p

Integrated Modeling Framework.

<p>Policies influence landowner decision-making, the effect of which depends on the different landowner types’ respective value systems. Landowner decisions affect habitat quantity and configuration, which function as inputs for the Grassland Bird Population Model.</p

A Novel Role for Keratin 17 in Coordinating Oncogenic Transformation and Cellular Adhesion in Ewing Sarcoma

Oncogenic transformation in Ewing sarcoma is caused by EWS/FLI, an aberrant transcription factor fusion oncogene. Glioma-associated oncogene homolog 1 (GLI1) is a critical target gene activated by EWS/FLI, but the mechanism by which GLI1 contributes to the transformed phenotype of Ewing sarcoma was unknown. In this work, we identify keratin 17 (KRT17) as a direct downstream target gene upregulated by GLI1. We demonstrate that KRT17 regulates cellular adhesion by activating AKT/PKB (protein kinase B) signaling. In addition, KRT17 is necessary for oncogenic transformation in Ewing sarcoma and accounts for much of the GLI1-mediated transformation function but via a mechanism independent of AKT signaling. Taken together, our data reveal previously unknown molecular functions for a cytoplasmic intermediate filament protein, KRT17, in coordinating EWS/FLI- and GLI1-mediated oncogenic transformation and cellular adhesion in Ewing sarcoma